ABSTRACT
Essentials ARHGEF10 single-nucleotide polymorphism provides risk of ischemic and atherothrombotic stroke. The role of ARHGEF10 in platelet function was examined using ARHGEF10 knockout mice. ARHGEF10 deficiency inhibits platelet function and arterial thrombus formation. ARHGEF10 knockout protects mice from stroke-induced infarction. SUMMARY: Background ARHGEF10, a member of the Rho guanine nucleotide exchange factor (GEF) family, stimulates Rho GTPases. Rho GTPases have been reported to regulate a variety of cellular behaviors, such as cell polarity, cytoskeletal organization, and gene transcription. ARHGEF10 single-nucleotide polymorphisms are linked to the risk of ischemic stroke. However, the role of ARHGEF10 in platelet function remains unknown. Objective To examine the role of ARHGEF10 in platelet function. Methods ARHGEF10-/- were generated. We examined the in vitro and in vivo effects of ARHGEF10 knockout on platelet function and arterial thrombosis formation. Results ARHGEF10-/- mice had normal platelet counts, but showed altered aggregation in response to thrombin, collagen, ADP, protease-activated receptor-4 peptide, and U46619 stimulation. ARHGEF10 knockout influenced platelet spreading on fibrinogen-coated surfaces, and caused the platelets to show less lamellipodia-like extension than wild-type platelets. ARHGEF10 knockout also inhibited platelet clot retraction induced by thrombin stimulation. ARHGEF10 knockout resulted in prolonged tail bleeding time and inhibited the stable thrombus formation induced by FeCl3 in the carotid artery. Conclusions ARHGEF10 serves as an important regulator in platelet shape change, spreading, and aggregation. Moreover, ARHGEF10 also plays an important role in arterial thrombosis formation.
Subject(s)
Arterial Occlusive Diseases/prevention & control , Blood Platelets/metabolism , Carotid Artery Diseases/prevention & control , Hemostasis , Platelet Aggregation , Rho Guanine Nucleotide Exchange Factors/deficiency , Thrombosis/prevention & control , Animals , Arterial Occlusive Diseases/blood , Arterial Occlusive Diseases/genetics , Carotid Artery Diseases/blood , Carotid Artery Diseases/genetics , Cell Shape , Chlorides , Disease Models, Animal , Ferric Compounds , Gene Knockout Techniques , Genotype , Male , Mice, 129 Strain , Mice, Knockout , Myosin Light Chains/metabolism , Phenotype , Phosphorylation , Platelet Glycoprotein GPIIb-IIIa Complex/metabolism , Rho Guanine Nucleotide Exchange Factors/blood , Rho Guanine Nucleotide Exchange Factors/genetics , Selenoprotein P/blood , Thrombosis/blood , Thrombosis/genetics , Time FactorsABSTRACT
Carcinosarcoma is a rare tumor with both malignant epithelium and interstitial components. Tumor entities have been described in many epithelial organs such as the lung, uterus, ovary, prostate and so on. Hypopharyngeal carcinosarcoma is extremely rare. Now we report a case of hypopharyngeal carcinosarcoma in our department in August of 2016 as follows.
Subject(s)
Carcinosarcoma/diagnosis , Hypopharyngeal Neoplasms/diagnosis , Female , Humans , Hypopharynx , MaleABSTRACT
HOXD gene cluster maps to chromosome 2q31 and plays a key role in embryonic limb morphogenesis. Mutations of the HOXD13 and HOXD10 genes have been found to be associated with digital and limb malformations. In addition, dysregulation of HOXD gene cluster has been proposed to account for the limb abnormalities in patients with chromosome 2q rearrangements. In this report, we investigated a three-generation family presenting clinical phenotypes of duplication of great toes, tapering fingers, and clinodactyly of the fifth finger in both hands, which were transmitted in a dominant fashion in this family. We identified and validated an interstitial microdeletion of approximately 3.4 Mb at chromosome 2q31.1-31.2 by array-based comparative genomic hybridization, fluorescence in situ hybridization, and real-time quantitative polymerase chain reaction that cosegregates with the clinical phenotypes in this family. The microdeletion removes 30 labeled genes including the entire HOXD gene cluster, suggesting that the digital abnormalities of this family may be attributed to the haploinsufficiency of the HOXD gene cluster. The delineation of the microdeletion region may contribute to the genotype-phenotype correlation study in patients with genomic rearrangements of the long arm of chromosome 2 and helps to understand the pathogenesis of haploinsufficiency of the HOXD gene cluster.
Subject(s)
Abnormalities, Multiple/genetics , Chromosome Deletion , Chromosomes, Human, Pair 2/genetics , Fingers/abnormalities , Toes/abnormalities , Child, Preschool , Family , Female , Foot Deformities, Congenital/genetics , Hand Deformities, Congenital/genetics , Homeodomain Proteins/genetics , Humans , In Situ Hybridization, Fluorescence , Karyotyping , Pedigree , Psychomotor Disorders/genetics , Transcription Factors/geneticsABSTRACT
We propose a novel multipurpose watermarking scheme, in which robust and fragile watermarks are simultaneously embedded, for copyright protection and content authentication. By quantizing a host image's wavelet coefficients as masking threshold units (MTUs), two complementary watermarks are embedded using cocktail watermarking and they can be blindly extracted without access to the host image. For the purpose of image protection, the new scheme guarantees that, no matter what kind of attack is encountered, at least one watermark can survive well. On the other hand, for the purpose of image authentication, our approach can locate the part of the image that has been tampered with and tolerate some incidental processes that have been executed. Experimental results show that the performance of our multipurpose watermarking scheme is indeed superb in terms of robustness and fragility.
ABSTRACT
The rate of glucose oxidation of fresh corneas of guinea pigs at different ages has been determined. Full-thickness corneal discs, 4 mm in diameter, were incubated in radioactive glucose solution. The quantity of the released CO2 was expressed in terms of the corneal discs, their dry weights, and DNA and protein contents. The rate of glucose metabolized to CO2 per hour was about 300 pmol/microgram DNA for guinea pigs weighing approximately 800 g. Glucose oxidation decreased as the age of the animals increased. Our results compared well with those obtained in other species. We therefore feel that the guinea pig should be a suitable model for research on the metabolism of corneas.
